Alcoholic Hepatitis (AH) is a major cause of liver-related morbidity and mortality. There are currently no approved therapies for severe AH. Two key barriers to drug development for severe AH are: (i) the high frequency of infection and sepsis which exclude most patients from clinical trials and is yet a major cause of mortality in this population, and (ii) the high rates of continued alcohol consumption after recovery from the acute illness that drives long-term mortality and re-hospitalization rates. In response to RFA-AA-18-005, we propose two pilot studies to begin to tackle these barriers. This will be accomplished by two sequentially performed trials as follows: Aim 1: To provide ?proof of concept? that high-dose ascorbic acid (AscA) administered intravenously along with antibiotics to subjects with AH who have active infection and sepsis is well-tolerated, safe, reduces systemic inflammation and is potentially effective for the treatment of AH. This is based on strong preliminary data indicating that AscA reduces inflammation and progression to multi-organ dysfunction in those with severe sepsis. Given that AH is associated with severe inflammation, we will test the possibility that AscA may provide common therapy for both AH and sepsis. We will test a fixed dose established to be safe and potentially effective in severe sepsis, a comparably sick population to those with AH and sepsis to evaluate its safety, tolerability, ability to reduce systemic inflammation and to generate preliminary data on its ability to reduce progression to multi-organ failure, as assessed by a 2-point worsening of the SOFA score. These studies will innovate by repurposing AscA from its use in severe sepsis to AH with infection, a condition excluded from virtually all AH clinical trials. Aim 2: To provide ?proof of concept? that lorcaserin, a 5HT2CR agonist, is well tolerated, reduces behavioral laboratory measured impulsivity, and enhances brain connectivity related to response inhibition and alcohol cue reactivity, and these changes correlate with reduction in alcohol use in survivors of AH. We will generate data on the safety, tolerability and efficacy of lorcaserin to reduce impulse control and related brain connectivity in those recovering from AH. We will also generate data on any effects of lorcaserin on alcohol consumption. This leverages our early data indicating that the 5HT2CR regulates impulsivity and associated alcohol consumption. Subjects recovering from a bout of AH requiring hospitalization will be enrolled 30-90 days after initial admission from AH. Thirty AH participants will be randomized to lorcaserin (10 mg twice a day by mouth) or placebo for four weeks. All participants will undergo two MR imaging sessions, one at baseline and one after four weeks of treatment with lorcaserin or placebo. Alcohol consumption will be measured at baseline, during treatment, and followed for one month after withdrawal from treatment to obtain preliminary data on effects of lorcaserin on alcohol consumption using alcohol timeline follow back questionnaires, serum phosphatidyl ethanol testing, and confirmation from family members. fMRI data will be related to alcohol consumption data. Trough levels of lorcaserin will be related to adverse events as well as alcohol consumption data.